Molecular Targets of Thymoquinone Protection Against Cisplatin-Induced Organ Toxicity: A Literature Review

Abstract

Cisplatin provides successful results against cancer, but its clinical use is very limited due to serious side effects in the form of toxicity to various organs. Thymoquinone has been shown to function as a scavenger of free radicals generated after nerve damage and has antioxidant, anti-inflammatory, and anti-apoptotic effects. This article provides a review of molecular targets of thymoquinone protection against cisplatin-induced organ toxicity. The study used the literature review method with article searches on four databases, namely Pubmed, Google Scholar, ScienceDirect, and the Cochrane Library. The search process for articles using keywords, including related word synonyms and MESH. Cisplatin toxicity occurs through a cycle driven by increased oxidative stress, inflammation, and apoptosis. Cisplatin has serious side effects in the form of toxicity to several organs, including ototoxicity, gastrointestinal toxicity, nephrotoxicity, and hepatotoxicity. Thymoquinone was shown to have antioxidant, anti-inflammatory, and anti-apoptotic effects. There are several molecular targets that play an important role in the protection of thymoquinone against cisplatin toxicity, including antioxidant enzymes (SOD, CAT, GSH-Px, GST), anti-inflammatory cytokines (TNF-α, IL-1, IL-2, IL-6, IL-10, NF-kB), anti-apoptotic and apoptotic protein (Bcl-2, Bax, caspase-3, caspase-8, caspase-9).